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from those associated with von Hippel-Lindau disease by unifocality, negative family history, and the absence of large dilated tortuous feeder vessels. 5 The exact cause is unknown, although it has been proposed that they could be expressions of vascularization of pigment epithelial proliferation or reactive gliosis. 5 We postulate that in the setting of chronic ROP and familial exudative vitreoretinopathy, there is retinal ischemia that produces a microenvironment conducive to vascular proliferation.Ophthalmologists who care for patients with a history of ROP should be aware of this late sequela because it is responsive to treatment and may cause additional vision loss.This lesion may be underreported because it may be difficult to identify in the setting of fibrotic residua and tractional elements.We recommend fluorescein angiography if new retinal thickening or exudates are seen in order to identify treatable lesions.In this case, we were able to identify the lesion before massive exudation occurred.Treatment options include laser photocoagulation, cryotherapy, photodynamic therapy, and, more recently, antivascular endothelial growth factor such as bevacizumab. 7,
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Rebecca B. Mets (2011) studied this question.
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